Neural control of ventricular rate in ambulatory dogs with pacing-induced sustained atrial fibrillation.

BACKGROUND: We hypothesize that inferior vena cava-inferior atrial ganglionated plexus nerve activity (IVC-IAGPNA) is responsible for ventricular rate (VR) control during atrial fibrillation (AF) in ambulatory dogs. METHODS AND RESULTS: We recorded bilateral cervical vagal nerve activity (VNA) and IVC-IAGPNA during baseline sinus rhythm and during pacing-induced sustained AF in 6 ambulatory dogs. Integrated nerve activities and average VR were measured every 10 seconds over 24 hours. Left VNA was associated with VR reduction during AF in 5 dogs (from 211 bpm [95% CI, 186-233] to 178 bpm [95% CI, 145-210]; P<0.001) and right VNA in 1 dog (from 208 bpm [95% CI, 197-223] to 181 bpm [95% CI, 163-200]; P<0.01). There were good correlations between IVC-IAGPNA and left VNA in the former 5 dogs and between IVC-IAGPNA and right VNA in the last dog. IVC-IAGPNA was associated with VR reduction in all dogs studied. Right VNA was associated with baseline sinus rate reduction from 105 bpm (95% CI, 95-116) to 77 bpm (95% CI, 64-91; P<0.01) in 4 dogs, whereas left VNA was associated with sinus rate reduction from 111 bpm (95% CI, 90-1250) to 81 bpm (95% CI, 67-103; P<0.01) in 2 dogs. CONCLUSIONS: IVC-IAGPNA is invariably associated with VR reduction during AF. In comparison, right or left VNA was associated with VR reduction only when it coactivates with the IVC-IAGPNA. The vagal nerve that controls VR during AF may be different from that which controls sinus rhythm.

Formation of the azygos vein / Formación de la vena ácigos

The aim of the present study was to determine the most common origin of the azygos vein. Thirty cadavers male and female, white and non-white adult individuals of different ages fixed in 10 percent formaldehyde and dissected. All cadavers had an undisclosed clinical death and were donated to the Universidade Estadual de Ciências da Saúde de Alagoa s, Brazil. Eleven different formations were found. The right subcostal vein was was only observed in 13 cases (43.33 percent); the azygos vein was formed by the confluence of the right subcostal and right ascending lumbar vein in three cases (10 percent); by the right subcostal vein with a contribution from the inferior vena cava (IVC) in three cases (10 percent); by the right subcostal with contribution from IVC and right ascending lumbar vein in three cases (10 percent); by the right and left subcostal veins in two cases (6.66 percent); by the right and left subcostal veins and contribution from the IVC in one case (3.33 percent); by the right and left subcostal veins and left accessory renal vein in one case (3.33 percent); by the left renal vein in one case (3.33 percent); by the right subcostal and left gonadal veins with contribution from the IVC in one case (3.33 percent); by the right subcostal and left renal veins in one case (3.33 percent); and composed by the continuation of the 11th posterior intercostal vein in one case (3.33 percent). Based on the results, the right subcostal vein was the only structure with a significant presence in the formation of the azygos vein.

El objetivo del estudio fue verificar cual es la disposición más frecuente del origen de la vena ácigos. Fueron disecados 30 cadáveres de individuos adultos, de ambos sexos, de diferentes grupos étnicos, fijados en formaldehído al 10 por ciento, donados a la Universidade Estadual de Ciencias da Saúde de Alagoas. Se encontraron 11 formaciones diferentes. En 13 casos (43,33 por ciento) se observó sólo la vena subcostal derecha; en 3 casos (10 por ciento) la vena ácigos estaba formada por la confluencia de las venas subcostal derecha y lumbar ascendente derecha; en 3 casos (10 por ciento) formado por las venas subcostal derecha y una contribución de la vena cava inferior VCI; en 3 casos (10 por ciento) por las venas subcostal derecha y contribución de la VCI y lumbar ascendente derecha; 2 casos (6,66 por ciento) por las venas subcostales derecha e izquierda; en 1 caso (3,33 por ciento) por las venas subcostal derecha, izquierda y contribución de la VCI; en 1 caso (3,33 por ciento) por las venas subcostal derecha e izquierda y renal accesoria izquierda; en 1 caso (3,33 por ciento) por la vena renal izquierda; en1 caso (3,33 por ciento) por las venas subcostal derecha, gonadal izquierda y contribución de la VCI; en 1 caso (3,33 por ciento) por las venas subcostal derecha y renal izquierda y en 1 caso (3,33 por ciento) por la continuación de la 11 vena intercostal posterior. Con base en los resultados podemos concluir que la vena subcostal derecha fue la única estructura con presencia significativa en la formación de la vena ácigos.

Aspectos biométricos y morfológicos del pericardio fibroso y diafragma en el hombre / Biometric and morphological charachteristics of the fibrous pericardium and the diaphragm in man

El pericardio es una membrana fibro-serosa que envuelve al corazón y a la porción yuxtacardíaca de los grandes vasos. Realizamos un estudio del pericardio y del diafragma, registrando sus dimensiones, sus relaciones, así como también, establecer el tipo de conexiones existente entre ambas estructuras. Fueron disecadas 142 regiones mediastínicas de cadáveres sin fijación o con fijación en formaldehído al 10 por ciento, brasileños, adultos, de ambos sexos, de edades comprendidas entre los 18 y 70 años, fallecidos de diferentes causas. Para el estudio histológico, del conjunto pericardio y diafragma fueron retirados cinco fragmentos de diferentes regiones: anterior próxima al esternón (región 1), lateral izquierda próxima al ápice del corazón (región 2), posterior (región 3), lateral derecha próxima al paso de la vena cava inferior (región 4) y central (región 5). El promedio de los diámetros latero-lateral y antero-posterior del pericardio fueron de 103,3 +/- 6,7 y 66,0 +/- 2,3 mm, respectivamente y del diafragma de 309,4 +/- 27,4 y 152,5 +/- 24,9 mm, respectivamente. El área del diafragma fue en promedio de 37. 260 +/- 2.324 mm2. El área de la base del pericardio sobre el diafragma fue de 6.042 +/- 367 mm2. El espesor del diafragma fue en promedio: parte derecha, 2,42 +/- 0,34 mm; parte izquierda, 2,38 +/- 0,71 mm y la parte anterior, 2,52 +/- 0,66 mm. El promedio del espesor del pericardio separado del diafragma fue de 0,26 +/- 0,02 mm. En la región 2 ambas estructuras fueron separadas con facilidad en 47,2 mm; en la región 5 ambas estructuras se encuentran fusionadas. Los resultados obtenidos en este trabajo complementarán los conocimientos morfológicos sobre el pericardio fibroso y sus relaciones con el diafragma.

The pericardium is a fibrous and serous membrane that surround the heart and the juxta- cardiac portion of the great vessels. We studied the pericardium and diaphragm and we recorded different measurements, relations and connection between both. We dissected 142 mediastinal regions from 10 percent formaldehyde ¡ fixed or fresh individual cadavers, Brazilian adults, of both sexes, from 18-70 years of age. For the histology study from both structures were sectioned five fragments of different regions: anterior, next to sternum (region 1), left lateral, next to heart apex (region 2), posterior (region 3), right lateral, next to course of inferior vena cava (region 4) and central(region 5). The average of transversal and anterior-posterior diameters of pericardium were 103.3 +/- 6.7 mm and 66.0 +/- 2.3 mm, respectively; the same diameters of diaphragm were 309.4 +/- 27.4 mm and 152.5 +/- 24.9 mm, respectively. The diaphragm area was 37,260 +/- 2,324 mm² and the area of pericardium base over the diaphragm was 6,042 +/- 367 mm² . The thickness of diaphragm was 2.42 +/- 0.34 mm in right part, 2.38 +/- 0.71 mm in left part and 2.52 +/- 0.66 mm in anterior part. The thickness of pericardium was 0.26 +/- 0.02 mm. In region 2 both structures were easily separated in 47.2 mm; in the region 4 both structures are fused. The results of this study will complement the morphologic knowledges about fibrous pericardium and its relationships with the diaphragm.

A rare Lymphatico-Venous communication associated with duplication of thoracic duct

RESUMEN: Una inusual presentación de duplicación del conducto torácico con una rara comunicación linfático-venosa, fue encontrada durante una disección de rutina, por estudiantes de pregrado. El conducto torácico se encuentra duplicado a nivel de la vértebra T12. Normalmente el conducto torácico se abre en la unión de la venas yugular interna izquierda y subclavia izquierda. En el lado derecho del cuello, el conducto linfático derecho recibe la linfa de la parte derecha de la cabeza y del cuello, del miembro superior derecho y lado derecho del tórax. El conducto torácico duplicado en el lado izquierdo se abrió directamente en la vena cava inferior. Este caso es discutido con respecto a su desarrollo, incidencia y significación clínica.

Differential involvement of N-type calcium channels in transmitter release from vasoconstrictor and vasodilator neurons.

1. The effects of calcium channel blockers on co-transmission from different populations of autonomic vasomotor neurons were studied on isolated segments of uterine artery and vena cava from guinea-pigs. 2. Sympathetic, noradrenergic contractions of the uterine artery (produced by 200 pulses at 1 or 10 Hz; 600 pulses at 20 Hz) were abolished by the N-type calcium channel blocker omega-conotoxin (CTX) GVIA at 1-10 nm. 3. Biphasic sympathetic contractions of the vena cava (600 pulses at 20 Hz) mediated by noradrenaline and neuropeptide Y were abolished by 10 nm CTX GVIA. 4. Neurogenic relaxations of the uterine artery (200 pulses at 10 Hz) mediated by neuronal nitric oxide and neuropeptides were reduced <50% by CTX GVIA 10-100 nm. 5. Capsaicin (3 microm) did not affect the CTX GVIA-sensitive or CTX GVIA-resistant neurogenic relaxations of the uterine artery. 6. The novel N-type blocker CTX CVID (100-300 nm), P/Q-type blockers agatoxin IVA (10-100 nm) or CTX CVIB (100 nm), the L-type blocker nifedipine (10 microm) or the 'R-type' blocker SNX-482 (100 nm), all failed to reduce CTX GVIA-resistant relaxations. The T-type channel blocker NiCl(2) (100-300 microm) reduced but did not abolish the remaining neurogenic dilations. 7. Release of different neurotransmitters from the same autonomic vasomotor axon depends on similar subtypes of calcium channels. N-type channels are responsible for transmitter release from vasoconstrictor neurons innervating a muscular artery and capacitance vein, but only partly mediate release of nitric oxide and neuropeptides from pelvic vasodilator neurons.

No involvement of the AT2-receptor in angiotensin II-enhanced sympathetic transmission in vitro.

Angiotensin II (Ang II) enhances sympathetic neurotransmission via AT(1)-receptors located on sympathetic nerve terminals. We recently demonstrated that inhibition of Ang II-mediated facilitation in the pithed rat by irbesartan resulted in a U-shaped dose response curve, which was not observed when PD 123319, at a concentration that selectively blocks the AT(2)-receptor, was co-administered. Hence, the irbesartan-mediated upstroke might be explained by the involvement of the AT(2)-receptor after AT(1) blockade with high-dose irbesartan. In the present study, we further investigated the possible role of the AT(2)-receptor in Ang II-mediated facilitation in vitro. We studied the effect of the AT(2)-receptor antagonist PD 123319 (10 nM) on Ang II-enhanced sympathetic outflow evoked by electrical field stimulation (EFS) in the rat isolated inferior vena cava. Additionally, we investigated the effect of the AT(1)-receptor blocker irbesartan (0.1 nM 1 M) on the sequelae of Ang II-enhanced, EFS-evoked sympathetic nerve traffic in the presence or absence of PD 123319 (10 nM). PD 123319 did not influence Ang II-enhanced sympathetic outflow. Irbesartan dose-dependently attenuate Ang II-augmented transmitter release (pIC50 7.99+0.03), whereas no U-shaped concentration-response relationship for irbesartan was observed. Co-administration of PD 123319 with irbesartan proved unable to influence Ang II-mediated facilitation differently compared with irbesartan alone. The experimental observations indicate that the AT(2)-receptor is not involved in Ang II-mediated enhancement of sympathetic nerve traffic in the present in vitro study.

Botulinum neurotoxin A attenuates release of norepinephrine but not NPY from vasoconstrictor neurons.

We examined effects of botulinum neurotoxin A (BoNTA) on sympathetic constrictions of the vena cava and uterine artery from guinea pigs to test the role of soluble NSF attachment protein receptor (SNARE) proteins in release of the cotransmitters norepinephrine (NE) and neuropeptide Y (NPY). Protein extracts of venae cavae and uterine arteries showed partial cleavage of synaptosomal associated protein of 25 kDa (SNAP-25) after treatment in vitro with BoNTA (50-100 nM). The rising phase of isometric contractions of isolated venae cavae to field stimulation at 20 Hz, mediated by NE acting on alpha-adrenoceptors, was reduced significantly by 100 nM BoNTA. However, sustained sympathetic contractions mediated by NPY were not affected by BoNTA. In uterine arteries, noradrenergic contractions to 1-Hz stimulation were almost abolished by BoNTA, and contractions at 10 Hz were reduced by 50-60%. We conclude that SNARE proteins are involved in exocytosis of NE from synaptic vesicles at low frequencies of stimulation but may not be essential for exocytosis of NPY and NE from large vesicles at high stimulation frequencies.

[Treatment of tachycardic atrial fibrillation by catheter-assisted electrical stimulation of the cardiac parasympathetic nervous system]. / Die Behandlung des tachykarden Vorhofflimmerns durch kathetergestützte elektrische Stimulation des kardialen parasympathischen Nervensystems.

UNLABELLED: Treatment of tachycardic atrial fibrillation (AF) is difficult in patients with congestive heart failure because many drugs which exert negative dromotropic effects (beta-blockers, calcium channel antagonists) may depress ventricular contractility and/or decrease arterial blood pressure. We have identified 2 intravascular sites in the superior (SVC) and inferior vena cava (IVC) where parasympathetic nerves, which innervate the atrioventricular node, can be stimulated electrically. In 8 dogs, a 7-F catheter with an expandable electrode basket at its tip was non-fluoroscopically positioned in the SVC and in the proximal IVC (time for positioning: 3-5 minutes). High-frequency electrical parasympathetic stimulation (PS) with 20 Hz at an impulse duration of 0.1 ms was performed during pacing induced AF. RESULTS: With increasing stimulus strength, a graded ventricular rate slowing was observed during PS in the SVC and IVC (P < 0.01, ANOVA). The negative dromotropic effect started instantaneously after onset of PS and ceased immediately after termination of PS. During ventricular pacing at a constant rate, no decrease of the arterial blood pressure was observed during PS. PS in the IVC yielded significantly lower stimulation thresholds than in the SVC. CONCLUSIONS: Transvenous parasympathetic stimulation for ventricular rate control during AF can easily be achieved in the SVC and IVC in dogs. This procedure may provide a foundation for investigating the usefulness of PS in humans. If the results translate to patients, PS may be very beneficial in the treatment of AF in patients with congestive heart failure.

Hepatic vein, hepatic parenchymal, and inferior vena caval mechanoreceptors with phrenic afferents.

Dogs were anesthetized with pentobarbital sodium and placed on positive-pressure ventilation. The right phrenic nerve and/or its C5 branch were prepared for afferent recording. The hepatic veins, hepatic parenchyma, diaphragm, and inferior vena cava were studied for mechanoreceptors using light pressure and stroking as the stimuli. Mechanosensitive areas were found in the hepatic veins, hepatic parenchyma of the right medial lobe, and inferior vena cava. The hepatic vein and inferior vena caval receptors are located in the same 1- to 2-cm region as the sphincters that are found in these vessels. This study presents the first experimental evidence for the existence of hepatic vein receptors, hepatic parenchymal receptors, and inferior vena caval mechanoreceptors with phrenic afferents in the dog. These sensory areas of the circulation may be involved in the neural control of venous return as well as mediating changes in intrahepatic and portal venous blood pressure during normal respiration.

Catheter ablation of atrial flutter circuits.

Atrial flutter (AF) mapping has shown circular activation in the right atrium (RA), with a "counterclockwise" rotation in a frontal view. The myocardial isthmus between the inferior vena cava and the tricuspid valve (IVC-T) closes the activation circuit in its caudal end. The reproducibility of this activation pattern, and the fact that some "rare" AF with a "clockwise" rotation of activation use the same circuit, suggests that reentry is greatly facilitated by the anatomical arrangement of the caudal end of the RA. This suggested that ablation of the IVC-T isthmus may interrupt AF and prevent its recurrence. We have applied radiofrequency (RF) current to the IVC-T isthmus in nine patients, producing sudden interruption of activation at this point in five (all those treated with large surface electrode catheters). In three others, RF produced acceleration or disorganization, leading to interruption. Preliminary follow-up data suggest a favorable effect on AF recurrence, either by preventing it, or by making antiarrhythmic drugs effective.

Inhibition of noradrenaline release in the rat vena cava via prostanoid receptors of the EP3-subtype.

1. In segments of the rat vena cava preincubated with [3H]-noradrenaline and superfused with physiological salt solution (containing desipramine and corticosterone), we studied the effects of prostaglandins of the D, E and F series, of a prostacyclin analogue and a thromboxane-mimetic and of subtype-selective prostaglandin E-receptor (EP-receptor) ligands on the electrically (0.66 Hz)-evoked tritium overflow. 2. The electrically-evoked tritium overflow was inhibited by prostaglandin E2 (maximum inhibition by about 80%; pIC40 7.49). The effect of prostaglandin E2 was not affected by rauwolscine, which, by itself, increased the evoked overflow; the alpha 2-adrenoceptor antagonist was added to the superfusion medium in all subsequent experiments. Indomethacin failed to affect either the evoked tritium overflow or its inhibition by prostaglandin E2. 3. The inhibitory effect of prostaglandin E2 on the electrically-evoked tritium overflow was not altered by the EP1-receptor antagonist. AH 6809 (6-isopropoxy-9-oxoxanthene-2-carboxylic acid) at a concentration at least 30 fold higher than its pA2 value at EP1-receptors. The following compounds mimicked the effect of prostaglandin E2 showing the following rank order of potencies: misoprostol (EP2-/EP3-receptor agonist) congruent to sulprostone (EP1-/EP3-receptor agonist) congruent to prostaglandin E1 = prostaglandin E2 >> iloprost (EP1-/IP-receptor agonist) = prostaglandin F2 alpha. The evoked overflow was not affected by high concentrations of prostaglandin D2 or the thromboxane-mimetic U46619 (9,11-dideoxy-11 alpha, 9 alpha-epoxy-methano-prostaglandin F2 alpha). 4. The present results suggest that the postganglionic sympathetic nerve fibres innervating the rat vena cava are endowed with presynaptic EP3-receptors.They are not tonically activated by endogenously formed products of cyclo-oxygenase and do not interact with the presynaptic M2-adrenoceptors.

Mutual interaction between presynaptic alpha 2-adrenoceptors and 5-HT1B receptors on the sympathetic nerve terminals of the rat inferior vena cava.

Segments of the rat vena cava preincubated with [3H]noradrenaline and superfused with [3H]noradrenaline-free solution containing desipramine and corticosterone were stimulated electrically (standard parameters: 150 mA, 0.3 ms, 0.66 Hz; duration 6 min). In some experiments the stimulation parameters were modified in order to obtain similar absolute release values despite the presence of an alpha-adrenoceptor agonist or antagonist or of 5-hydroxytryptamine (5-HT). In a first set of experiments, the vascular segments were first exposed to an alpha-adrenoceptor ligand, which was kept present throughout the remainder of superfusion, and then to 5-HT. The release-inhibiting effect of 5-HT was attenuated by the alpha 2-adrenoceptor agonists clonidine and B-HT 920 whereas it was enhanced by the alpha-adrenoceptor antagonists phentolamine and idazoxan. The alpha 1-adrenoceptor antagonist prazosin did not change the 5-HT-induced inhibition of noradrenaline (NA) release. In a second set of experiments, 5-HT was administered first and kept present in the superfusion fluid for the remainder of the experiment. In the presence of 5-HT, the overflow-inhibiting effects of B-HT 920 and clonidine and the overflow-enhancing effect of idazoxan were reduced. The results demonstrate that activation of one kind of receptor decreased the inhibition of noradrenaline release produced by activation of the other. These effects were not the consequence of the change of release per se induced by the interacting drugs, since they also occurred when the release was adjusted to similar levels by modification of the stimulation parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Sequential changes of noradrenaline content of vein grafts in rats: quantitative estimation by high-performance liquid chromatography using electrochemical detection.

Supradiaphragmatic inferior vena cava was transplanted end-to-end into the abdominal aorta of 11-week-old rats of the same inbred strain and same litter using microvascular technique. The grafts were removed 3 days, 4, 8, 16, and 35 weeks postoperatively, and their noradrenaline (NA) content was estimated by high-performance liquid chromatography using electrochemical detection. The amount of NA was significantly lower (P less than .001) in all vein grafts as compared to nontransplanted vena cava. The substantial decrease of NA in the vein grafts throughout the observation period indicates a persistent denervation of the transplant.

Localization of vagal preganglionic somata controlling sinoatrial and atrioventricular nodes.

Canine cardiac vagal ganglia in the region of the inferior vena cava and inferior left atrium (IVC-ILA) and at the junction of the right pulmonary veins and left atrium (PVFP) control atrioventricular conduction and heart rate, respectively. After retrograde transport of horseradish peroxidase (HRP) injected separately into these ganglia in different dogs, the left and right and longitudinal distributions of brain stem somata terminating in these ganglia were compared with functional dominance of left and right vagal control of heart rate and atrioventricular conduction. Labeled somata innervating these ganglia had quite similar longitudinal distribution patterns. Although functional dominance of heart rate was found to be in either the right vagus or bilaterally in both vagi, a corresponding difference in somata innervating the PVFP ganglia was not found. Functional vagal dominance of atrioventricular conduction was found to be either right, bilateral, or left with correspondence between left-right distributions of somata after HRP injection into the IVC-ILA region. However, these results should be cautiously interpreted because these ganglia mediate other cardiac functions.

Excitatory cholinergic innervation in canine portal and mesenteric veins.

A possibility that the canine portal and mesenteric veins may have an excitatory cholinergic innervation similar to that observed in the middle segment of the inferior vena cava (IVC) was investigated. After adrenergic blockade with prazosin, contractile responses of isolated longitudinal strips of the portal and mesenteric veins to transmural electrical stimulation were greatly diminished. Subsequent anticholinesterase (neostigmine or physostigmine) treatment, however, revealed in the nerve-evoked contraction a component that was antagonized by atropine. The same phenomenon was also observed in circular strips of the portal and mesenteric veins but was absent in those of the external jugular, saphenous, and splenic veins. In accord with the results of nerve stimulation, concentration-response curves of acetylcholine-induced contraction were shifted leftward by neostigmine in strips of the portal and mesenteric veins as well as of the middle segment of IVC. In contrast, no shift was observed in 12 other different sites of the venous system. Cholinesterase staining demonstrated positively stained smooth muscle and nerve fibers in the portal and mesenteric veins and in the middle segment of IVC. These findings indicate the existence of excitatory cholinergic innervation in the portal and mesenteric veins, which may reflect the common embryological origin of smooth muscle of these veins with the intestinal muscle.

Inhibition of noradrenaline release via presynaptic 5-HT1B receptors of the rat vena cava.

In the rat inferior vena cava preincubated with 3H-noradrenaline, the effects of nine serotonin (5-HT) receptor agonists and of eight antagonists (including two beta-adrenoceptor blocking agents) on the electrically evoked 3H overflow were determined. 1. 5-HT, 5-carboxamido-tryptamine, 5-methoxy-3(1,2,3,6-tetrahydropyridine-4-yl)-1H-indole (RU 24969), 5-methoxytryptamine, N,N-dimethyl-5HT, tryptamine and 5-aminotryptamine inhibited the evoked 3H overflow. The potencies of these agonists in inhibiting overflow were significantly correlated with their affinities for 5-HT1B binding sites, but not with their affinities for 5-HT1A, 5-HT1C or 5-HT2 binding sites. 8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a 5-HT1A receptor agonist, and ipsapirone, a partial agonist at these receptors, did not inhibit overflow. 2. Cyanopindolol facilitated the evoked 3H overflow, an effect which was abolished by propranolol. The maximum inhibition of overflow obtainable with 5-HT was diminished by cyanopindolol. 3. The concentration-response curve for 5-HT was shifted to the right by metitepine, metergoline, quipazine, 6-chloro-2-(1-piperazinyl)pyrazine (MK 212) and propranolol which, given alone, did not affect 3H overflow. The apparent pA2 values of these antagonists tended to be correlated with their affinities for 5-HT1B (but not 5-HT1A, 5-HT1C or 5-HT2) binding sites. Ketanserin, a 5-HT2 receptor antagonist, and spiperone, which blocks 5-HT2 and 5-HT1A but not 5-HT1B or 5-HT1C receptors, failed to antagonize the effect of 5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

Parasympathetic ganglia innervating the canine atrioventricular nodal region.

Surgical disruption of the small (approximately 0.7 x 1.0 cm) epicardial fat pad situated at the junction of the inferior vena cava (IVC) and inferior surface of the left atrium (ILA) interrupts both right and left vagal input to the atrioventricular nodal (AVN) region of the canine heart. This intervention eliminates AV block during supramaximal stimulation of both cervical vagi, without interfering with sinus bradycardia normally associated with sinoatrial nodal (SAN) suppression. Independent modulation of SAN and AVN activities by the parasympathetic system is thereby revealed. Histology of the excised IVC-ILA fat pad reveals multiple well organized autonomic ganglia. These ganglia range from 2 to 80 cells per cluster and are associated with numerous nerve trunks. Individual ganglia are commonly surrounded by fatty connective tissue closely adjacent to epicardial muscle. They have not been found imbedded within atrial muscle and have been been found in or close to endocardial muscle layers. Other ganglia, imbedded in the fat pad overlying the posterior surface of the left atrium or in the atrioventricular groove, do not directly modulate A-V conduction. Surgical dissection around the extreme left or middle segments of the great cardiac vein and the coronary sinus failed to interrupt either left or right vagal input to the AVN region. Parasympathetic, preganglionic pathways to these AVN synapses do not, therefore, course from left to right along the atrioventricular groove. However, dissection around the extreme right portion of the coronary sinus at its penetration of the inferior interatrial septum, did interrupt vagal influences upon A-V conduction. Thus, numerous autonomic ganglia have been localized in the canine heart which serve as synaptic stations mediating both right and left vagal regulation of A-V conduction.

Selective vagal innervation of the heart.

Parasympathetic ganglia are imbedded (1) in the epicardial fat pad located on the posterior surface of the dog's heart and (2) immediately overlying the point of penetration by the coronary sinus into the interatrial septum. The fat pad is situated between the inferior vena cava and the inferior left atrium. It contains multiple encapsulated ganglia, each consisting of two to 80 separate cells, richly intermingled with neural elements. Destruction of these ganglia by surgical excision and/or phenol painting interrupts both right and left vagal inhibition of atrio-ventricular (A-V) conduction, without obviously altering vagal modulation of sinoatrial function. Excision or phenol destruction of the fat pad overlying the right pulmonary vein inlets to the left atrium interrupts both right and left vagal inhibition of sinoatrial function, again without interfering with vagal control of atrioventricular nodal function. Well organized, encapsulated autonomic ganglia are also found throughout this fat pad. These experiments thus identify and localize separate concentrations of ganglion cells which differentially modulate automaticity and A-V conduction in the canine heart.

[Neuronal activity of microganglia of the vena cava orifice]. / Neironal'naia aktivnost' mikrogangliev ust'ia polykh ven.

Spontaneous activity of ganglionic neurons was studied in vitro in subserous plexus of the isolated preparations of inferior vena cava segments attached to the ventricle. Presence of the active neurons along with the "silent" those was shown. Mechanosensitive neurons with a single response to mechanical stimulation constituted a separate group. The neurons under study belong to the metasympathetic part of the nervous system and are supposed to affect the functional state regulation of the intracardiac sinus node.